Motor Control of the cervical and lumbar spine

Motor Control considerations in the cervical spine

• Action cannot be considered as the sum of isolated movements • Control operations are very much dependent upon the goal of the movement • Cervical spine is not analogous to the rest of the spinal column due to it’s large degrees of freedom and specific inputs from intero- and extero-ceptors • Issues of control must also consider the redundancies (spare capacity) within the system • 20 pairs of muscles many of which can perform similar actions (Peterson et al 1989) • Ultimate degrees of freedom problem is how to reduce/simplify the movement to be as efficient as possible (Bernstein 1967) • Overall the number of independently controlled muscle elements (including compartmentalisation and subdivisions) exceeds the degree of freedom • Many neck muscles have multiple insertions and multiple functions whose variability is task dependent (Richmond et al 1991, 1992) • 8 joints with 6 degrees of freedom each – 3 rotational and 3 translational • Simplified the greatest degrees of freedom occur for rotation at C1/2, flexion C1/2, and extension 0/C1, lateral bending across all vertebrae • Head represents only 7% body weight but has 20 muscles linking the skull to the spine (Sherk & Parke 1983). The CNS programmes neck muscles to respond to specific directions of movement rather than generating an infinite variety of motor patterns (Keshner et al 1992) • Neck muscle morphometry reveals heterogeneity w.r.t. musculotendon, sarcomere, fascicle length, angles of pennation, muscle fibre type (density of I vs II), and instead of distinct tendons the muscles attached to bone through an architecturally complex internal tendon & aponeurosis (Kamibayashi & Richmond 1998)

Muscle layers

• Muscles arranged in layers with the outer layer connecting the skull and shoulder girdle, with the deeper layers linking cervical and thoracic vertebrae. • Superficial layer includes trapezius (whose fibres are sparse above C4) and sternocleidomastoid, the next layer include long dorsal (splenius capitis, semispinalis capitis and longissimus capitis) and long ventral (longus capitis), slightly deeper to this lie the splenius cervicis, semispinalis cervicis, longissimus cervicis and longus colli which link the vertebrae, • whilst the deepest layers are the suboccipital muscles which include the rectus capitis major/minor, obliquus capitus superior/inferior

Functional Synergies

• The problem of the controller is the optimisation between mobility and stability • Muscle synergy has been described as “a consistent grouping of muscles to accomplish a specific task” (Turvey et al 1982) i.e muscles spanning several joints yet acting as a single unit (Buchanan et al 1989) • Separate actions of 2 groups of muscle would assist the head-neck controller to meet the task of stability and movement (Thomsen et al 1994) • Several muscles can achieve the same direction of movement. The controlled parameter appears to be the required force vector rather than the specific force lever arm of any one muscle (Macpherson 1988, 1991) • In Rhesus monkeys during the upright position, muscle activation patterns were in functional groupings determined by their anatomical attachments, whereas in the quadrupedal position, gravity acting horizontally on the head produced greater activation and a collective response of the muscles suggesting a connection between central recruitment and the mechanical requirements of the task (Mayoux-Benhamou et al 1997) • A mathematical model of head-neck control (Peng et al 1996) has identified stiffness and the vestibulocollic reflex as the primary contributors for the stabilisation of the head in space • Vestibulocollic and cervicocollic reflexes respond reactively to acceleration and proprioceptive stimuli to orientate the head in space (VCR) maintain the head on trunk (CCR) • Voluntary responses are those required for tracking and are based on exteroceptive information (visual, auditory, olfactory) • Vestibulospinal pathways have monosynaptic and disynaptic descending inputs onto cervical motoneurones which have a distinct orienting function (Karlberg et al 1995). • Other descending pathways, particular the reticulospinal pathways have been shown to be equally important in eliciting the VCR response (Peterson1984)

Cervical Spine reflexes

• The VCR produces counter-rotation of the head on trunk during postural disturbances • The CCR stabilizes the head on the body and can provide information about the rotation of the head on the trunk • Recent findings (Gdowski & McCrea 2000) suggest that correct alignment of the head with the trunk and with the gravitoinertial vertical (Imai et al 2001) requires that the vestibular system receive ascending somatosensory inputs (Keshner 2005) • Semicircular canals are stimulated by angular acceleration in the horizontal plane • The evidence suggests the presence of more signal processing than expected from a monosynaptic pathway, with evidence of a pre-synaptic inhibition in the CCR response (Banovetz et al 1995) • The otoliths are stimulated by linear accelerations of the head and their inputs have been found to modify both eye and head stabilization (Schor et al 1985), however inputs from the otoliths cannot compensate perfectly to eye and neck responses (Borel & Lacour 1982) • It was proposed that compensatory head pitch movements were produced predominantly by the angular vestibocollic reflex at slow walking speeds and by linear vestibulocollic reflex at high speeds (Hirasaki et al 1999) • Sinusoidal stimulation in the horizontal and vertical planes (with the trunk fixed) indicate that at below 1Hz, the head is primarily stabilized by longer latency voluntary pathways observed as anticipatory torques in the neck muscles or responses controlled by visual signals, whereas at higher at frequencies, mechanical factors (e.g. inertia, stiffness and viscoelasticity) become important and act with little delay (Keshner 2005) • Linear translations with the trunk free to move, revealed a significant somatosensory component to head stabilization (Vibert et al 2001)

Motor control of the trunk

• ‘internal model of body dynamics’ – comparative centre of input to expectations evaluating the response • “Optimal trunk function is a complex interplay between movement and control of the integrity of the spine and pelvis at the intersegmental level, at a global level involving the control of orientation, and the contribution of the trunk to maintain equilibrium of the body w.r.t gravity and external forces” (Paul Hodges 2005) • Even static postures involve movement with small cyclical movements occurring to counter respiration (Hodges et al 2002) • Movement is used by the CNS to maintain stability and minimize energy expenditure e.g. small movements of the trunk prior to limb movements (Hodges et al 1999, 2000) and rotation of the pelvis around each orthogonal axis during gait (Perry 1992) • Models of stability must incorporate 3 levels of control

– Intersegmental control - orientation control - control of equilibrium

• Euler model of stability using buckling failure (90N)

– Argues that the activity and stiffness of antagonistic muscles is required for lumbar spine equilibrium – Considers muscles as ‘guy wires’ to stiffen the intervertebral joints that they span (Criso & Panjabi 1991) – Static consideration whereby few investigations have analysed this in dynamic terms (Cholewicki et al 1997)

• Beyond ‘buckling’, spinal health must consider control of global and intersegmental motion and the contribution of the trunk to postural equilibrium • Control of translation and rotation during an arc of movement (Bogduk et al 1995) must also be incorporated into a model of stability, where segmental control is an essential element (Crisco & Panjabi 1991) • Control of body equilibrium during changes in the centre of mass particularly in situations where there is a conflict between spinal orientation and balance through movement of the trunk

Principles of Motor Control

• ‘neutral zone’ is the area around the neutral position where minimal stiffness occurs (Panjabi 1992) • It has been argued that the ‘neutral zone’ increases in cases of chronic instability (Panjabi 1992) • Control elements

– Sensors – Control/planning system to analyse and prepare for execution – Muscles to execute the response

• Muscle elements to consider include

– redundancy – muscle architecture whereby muscles are biomechanically more suited to either motion or stability (Bergmark 1989; Richardson et al 1999, Sahrman 2002) – muscle function can be divided into extremes in the spectrum as well as medium spectrum function for

– Bergmark (1980) described muscles as either ‘global’ or ‘local’ based on anatomical characteristics

• Local muscles have limited ‘moment arm’ and cross one/few segments with an ideal anatomy to control intervertebral movement e.g. multifidus, intertransversarii and interspinalis, transverse abdominis • The global muscles have attachments to the pelvis and thorax and thus transcends multiple segments which have larger moment arms and therefore larger torques and hence function to orient the trunk and correct equilibrium e.g. erector spinae, lateral fibres of iliopsoas and quadratus lumborum, external and internal obliques, rectus abdominis • Synergy between local and global muscles is necessary for efficient movement. Excessive co-activation of global muscles can control shear and rotation, it can also lead increased compressive load on the intersegmental segments such as discs and joints

– posterior fibres of iliopsoas, medial fibres of quadratus lumborum, lumbar portions of longissimus and iliocostalis – Interspinalis and intertransversarii have a high density of muscle spindles suggesting a major proprioceptive rather than motor function (Nitz & Peck 1986) – Internal oblique has fibre orientation similar to transverse abdominis in the pelvis and may contribute to force closure of the SIJ (Snijders et al 1995)

Sensors

• Muscle spindles contain nuclear bag and nuclear chain fibres which are sensitive to muscle length and/or velocity of lengthening • The control component of these intrafusal muscle fibres allows the CNS to adapt the sensitivity of the spindle elements as well as to adapt the spindle to changes in muscle length • Alpha-gamma co-activation is essential for the perception of movement (Gandevia & McCloskey 1976) • Golgi-tendon organs provide inhibitory input to alpha motoneurons and attach to small populations of muscle fibres which make them sensitive to small forces thereby providing discrete detection of tension in different parts of the muscle (Houk & Simon 1967) • Joint receptors are encapsulated receptors (Ruffini and Pacinian corpuscles) which tend to fire at end of range when the joint is stretched (Nade et al 1987) • Ligamentous receptors and mechanoreceptors in the annulus of the disc whose electrical stimulation modulates activity in muscles of the spine including the multifidus (Indahl et al 1995) • Tactile receptors in the skin include Pacinian corpuscles, Meissner corpuscles, Merkel cells and Ruffini endings • Vestibular apparatus includes the saccule and utricle of the otoliths which detect the position of the head with respect to gravity, and the semicircular canals which detect acceleration of the head around three orthogonal axes • ?gravity receptor in the region of the kidneys? (Mittelstaedt 1996) • Visual and auditory

Controller

• Corticospinal input to the trunk muscles, course the spinal cord bilaterally or send collaterals to both sides (Kuypers 1981, Mori et al 1995) • More significant control of the trunk muscles by the brainstem such as the reticulospinal and vestibulospinal tracts which is consistent with the relatively small representation of the trunk muscles on the motor and sensory homunculii (Kuypers 1981) • The CNS has three primary strategies for the control of movement

– Feedforward and Open-loop strategies where the outcome of movement is predictable (e.g. ballistic and repetitive movements and predictable challenges to trunk control such as limb movements {Taub & Berman 1968}) – Closed-loop where sensory feedback is required in novel unpredictable tasks (Schmidt & Lee 1999) – Underlying level of tonic activity to increase muscle tension and hence stiffness acting as a line of defence against unexpected perturbations (Johansson et al 1991) using components of both feedforward and feedback strategies

• The CNS draws on the architectural characteristics of the trunk muscles to meet the concurrent demands of mobility and stability (Hodges 2005) • Motor programme theory

– Involves memory based mechanism whereby a generalized programme is stored as an abstract representation of a group of movements that are retrieved when movement is performed (Schmidt & Lee 1999) – The CNS store invariant features of movement such as sequence, timing, duration, relative force – However, Bernstein (1967) that too many degrees of freedom needed to be controlled concurrently for even the simplest movement

• Dynamic Pattern Theory (Kelso 1984)

– No central representation of all components of movement, but instead co-ordination is determined by environmental invariants and limb dynamics based on the principle of non-linear dynamics

Lumbo-pelvic stability

• Prediction based on an ‘internal system of body dynamics’ which is an abstract construct built up over a lifetime of movement experience and holds information about the interaction of internal and external forces (Gurfinkel 1994) • Parallel processing model for posture and movement (Massion 1992) • The temporal and spatial features of the superficial muscles are linked to the direction of forces acting on the spine (Aruin & Latash 1995; Hodges & Richardson 1997) and are therefore linked to orientation control • In contrast the deep muscles such as transverse abdominis and multifidus contract independent of the direction of movement and reactive forces (Moseley et al 2000) and therefore are link to intersegmental stability • Attention-demanding tasks produces a latency in the superficial muscle activation whereas no such latency was found in the deeper muscles (TrA Hodges & Richardson 1999, deep fibres of multifidus Moseley et al 2001) • The CNS predicts the amplitude and adjusts the feedforward response accordingly

Closed Loop control of the trunk

• Intended movement is compared against feedback regarding the status of the body and its relationship to the environment. If feedback differs from the intended movement an error signal is generated to correct the movement performance (Schmidt & Lee 1999) • May operate at a basic reflex level using mono-synaptic stretch reflexes for example short latency reflexes when catching an unexpected mass (Moseley et al 2001) which act ‘en masse’ with no differentiation between deep and superficial component (Moseley et al 2001). There appears to be some distant integration as loading or unloading of the arms can produce this trunk response and can be enhanced with predictability of the loading • Electrical stimulation of the SIJ in cats (Indahl et al 1999) and annulus fibrosis in pigs (Holm et al 2000) elicits short latency responses on both sides and over multiple segments.

Motor Control - Long loop reflexes

• Long latency involving processing at the cortical level and are thought to provide a greater role in error correction (Schmidt & Lee 1999). For instance when a supporting surface is suddenly removed, a complex interplay of several body parts, including responses of trunk muscles is activated in addition to using a hip or ankle strategy (Horak & Nashner 1986) • Used for long duration tasks that require accuracy whereby sensory information is used by the CNS to continually modulate movement performance in a goal directed manner

Control of muscle stiffness

• Muscle stiffness related to feedforward and feedback mechanisms provides joint support through the modulation of muscle tone and contributes to control even before the shortest reflex response could be initiated (Bergmark 1989; Johansson et al 1991)

Effect of Pain and Injury on Motor Control

Changes in open-loop control mechanisms • People in remission for their chronic low back pain demonstrated delayed onset of TrA with arm and leg movements in all directions (Hodges & Richardson 1996, 1998) • Data suggest that the responses are a result of inappropriate motor planning rather then changes in excitability or transmission of the command in the CNS (Hodges 2001)Changes in the closed loop control mechanism • Changes in all elements of the closed loop system have been reported. It is frequently difficult to determine whether the problem lies with inaccurate feedback from the periphery, inability to interpret feedback or inability to initiate an appropriate command (Hodges 2005) • Sensory deficit can be detected by measuring the acuity or smallest perceptible stimulation and to accurately copy a movement and return to a position after it has been demonstrated by the same or opposite limb – Impaired acuity to spinal motion in low back pain (Taimela et al 1999) and inability to reposition with low back pain (Gill & Callaghan 1998) has been demonstrated – This can lead to delayed reflex response as a result of increased time to reach a threshold response, faulty error detection and the development of a faulty ‘internal model of body dynamics’ – Muscle spindle sensitivity may also be altered by pain (Pederson et al 1997) • Afferent inputs may be misinterpreted in cases of hyperalgesia and allodynia • Changes in muscle activity may affect acuity (Gandevia et al 1992) and deep muscles attach to joint whereby contractions may affect sensation • Fatigue may also affect sensory acuity (Carpenter et al 1998) • Considerable debate as to the presence of augmented paraspinal muscle activity with some reporting increased (Wolf & Basmajian 1977, Arena et al 1989), reduced (Sihvonen et al 1997), asymmetrical (Cram & Steger 1983) and change in activity (Collins et al 1982) • Consistent finding of sustained erector spinae activity at end of range flexion when they would normally be inactive due to the ‘flexion-relaxation’ phenomenon (Shirado et al 1995, Zedka et al 1999, Kaigle et al 1998) and reduced relaxation during gait (Arendt-Nielsen et al 1996) • Delayed reduction in erector spinae muscles when the trunk is unloaded (Radebold et al 2000) • Further impairments seen are – balance when standing on one leg (Luoto et al 1998) or two legs (Byl & Sinnott 1991) or sitting (Radebold et al 2001) – increased risk of developing low back pain and recurrence has been shown in people with poor standing balance (Takala & Viikari-Juntura 2000) – people with low back pain having slower reaction times (Luoto et al 1995) which has been associated with predisposition to injuries in many sports (Taimela & Kujala 1992) – in multifidus fibre composition (Rantanen et al 1983), increased fatigability (Roy et al 1989, Biederman et al 1991) and reduced cross sectional area, identified as early as 24hours after the onset of acute unilateral low back pain (Hides et al 1994) • Therefore, the deep and superficial trunk muscles are affected in an opposite manner in the presence of pain

Effect of Pain and Injury on Motor Control

Motor control – cause or effect of dysfunction? • Changes of motor control can be as a result of pain or incompetent motor strategies lead to inefficient spinal control, thus microtrauma, nociceptive stimulation and pain (Janda 1978, Farfan 1973, Cholewicki et al 1997) • Studies have demonstrated changes in motoneuron excitability (Matre et al 1998), decreased cortical excitability (Valeriani et al 1999) and changes in sensitivity in muscle spindles (Pedersen et al 1997), • However, changes in motor planning and not simple inhibition or transmission delays have been suggested (Hodges 2001) and is consistent with the finding that pain changes the activity in the regions of the brain involved with motor planning (Derbyshire et al 1997) due to the attention demanding nature of pain or stress associated with pain thereby affecting limited resource processing capacity (Luoto et al 1999), however change in control of rapid arm movement tasks was not affected by attention-demanding nor stressful tasks (Moseley et al 2001) • Fear can replicate some features of the changes demonstrated in clinical and experimental pain (Moseley et al 2001)

Pain Adaptation Model

• Movement velocity and amplitude is reduced in the presence of pain (Lund et al 1991) • In the limb and jaw this is represented by reduced agonist and increased antagonist activity (Svensson et al 1995), in the trunk this may be represented by excessive splinting of the superficial muscles as predicted by Panjabi (1992) • Alternatively pain may affect motor control indirectly through its influence on proprioception, whereby in chronic pain non-nociceptive mechanoceptors contribute to afferent input on second order nociceptors thereby providing inaccurate feedback affecting feedforward responses due to a faulty ‘internal model of body dynamics’

Motor Control and Pain

• Under normal circumstances pain is the result of stimuli that either threaten or result in injury (Willis 1989) • Sensory – discriminative and motivational-affective pathways operate in parallel (Melzack & Casey 1968) • Even the memory of pain can condition behaviour “fear-avoidance’ which may serve a purpose to avoid further injury during acute pain but can be deleterious in chronic conditions. • The majority of investigations into pain have been done on cutaneous receptors which appear to act quite differently to deep receptors such as those from joints and muscle (Galea 2005) • Further difficulties arise in stimulus control as well as interpretation of motor behaviour due to the variety of conditions and the heterogeneity of the response • Muscle pain induced by an injection of a 5% solution of hypertonic saline (Kellgren 1938) appears to have similar behvioural manifestations as those seen clinically (Arendt-Nielsen et al 1996) • Cutaneous receptors terminate in lamina I & II of the dorsal horn, whereas deep receptors from muscle and joints terminate in lamina I and/or IV and V (Mense 1986, Hoheisel et al 1989) • Nociceptive specific neurones (NS) are found predominantly in lamina I and the outer part of lamina II, whereas wide-dynamic range (WDR) neurones are more concentrated in lamina V

Pain

• Convergence – Projection theory (Ruch 1946) is based on the multiplicity of overlap of receptive fields in the dorsal horn which may explain the referral of deep pain to cutaneous regions and the diffuse nature of deep pain sensations • The more medially located the cell is in the dorsal horn, the more distal is the site of the deep receptive field (Yu & Mense 1990) • Nociceptors are found throughout skeletal muscle but are most abundantly found in the tendons, fascia and aponeuroses (Stacey 1969) • Lesions of muscles can lead to release of endogenous sensitising substances such as kinins and prostaglandins which may cause oedema increasing pressure on the venous system resulting in ischaemia which promotes the release of Prostaglandin E2 and Bradykinin. Ischaemia may lead to failure of the calcium pump and local contracture further impairing circulation which is a theory behind the development of trigger points. • Sensitization of muscle tissue can lead to enhanced excitability of dorsal horn neurones which can cause central sensitization. • The ‘vicious cycle’ terminology has been given to the painful lesion stimulating gamma motoneurons which leads to enhanced muscle spindle sensitivity. Enhanced spindle activity activates the alpha motoneuron through a mono-synaptic reflex causing hypertonus of the affected muscle (Johansson & Sojka 1991) • Joint pain may arise from stimulation of nociceptors in the joint capsule, ligaments, bone, periosteum, articular fat pads and around blood vessels but not in the joint cartilage (Wyke 1981) • Increased background activity as well as increased activity to noxious and non-noxious movement in A beta, A delta and C fibres occur as a result of inflammation. ‘Silent nociceptors’ begin to respond in this scenario (Schaible & Schmidt 1988)

Pain & the Brain

• The thalamus represents the final link in the transmission of impulses to the cerebral cortex, processing almost all sensory and motor information prior to transfer to cortical areas • Spinothalamic afferents mediate sensory discriminative information and terminate in VPL nucleus and medial thalamic nuclei, whilst receiving extra information from the globus pallidus, reticular formation and the cerebellum (Galea 2002). Diffuse cortical projections from thalamic intralaminar nuclei have been considered as part of a non-specific arousal system. • The basal ganglia are associated with planned action (Brooks et al 1993) and movement (Colebatch et al 1991). Their connections through the thalamus, prefrontal cortex, supplementary motor cortex, motor cortex and anterior cingulate cortex (Cote & Crutcher 1991) form a circuit associated with motor preparation or response selection. • A number of brains stem structures, including peri-aqueductal grey matter (Bernard & Bandler 1998) and the reticular formation have extensive connections with all levels of the nervous system and are involved with nociceptive, autonomic and motor systems • Multiple cortical areas are activated by pain. These include the primary somatosensory cortex (Bushnell et al 1999), the secondary somatosensory cortex, the pre-frontal cortex, anterior cingulate cortex (Talbot et al 1991), and supplementary motor area (Coghill et al 1994) • Parietal areas are mainly concerned with sensory-discriminative aspects whereas frontal-limbic connections subserve the affective dimension of pain experience (Galea 2005) • There are corticospinal projections to all lamina of the dorsal horn from mainly post-central cortical areas, whereas pre-central cortical areas project to lamina VII and VIII, with neurones from the motor cortex projecting to lamina IX (Galea & Darian-Smith 1997, Maier et al 1997) • The majority of these descending projections terminate on interneurons which are part of the spinal circuit which means that the ‘sate’ of the interneuron is dependent upon the combined descending input, afferent input, and spinal interactions for the upcoming motor task • Corticospinal projections to the superficial lamina can modulate NS neurons (Cheema et al 1984) • Posterior parietal cortex has connections with primary somatosensory cortex and other polymodal associated areas, including the limbic system (Cavada & Goldman-Rakic) and is part of a general attentional system. • The cingulate cortex is involved in the affective and motor behaviours (Devinsky et al 1995). This region contains neurons which fire in anticipation of pain and therefore could be involved in avoidance behaviour (Koyama et al 1998) • The insula receives converging information from all 5 sensory modalities and has extensive connections with the limbic system and spinal cord (Galea 2002)

Pain & the Brain

Muscle hyperactivity and chronic pain • Facilitation of gamma reflex through group III and IV mechanoceptors and nociceptors in painful muscles was proposed by Johannson & Sojka (1991) • This facilitation in turn promotes excitation of group I and II afferents which influence the alphamotoneurons causing further contraction, possible ischaemia and release inflammatory metabolites such as Bradykinin and Prostaglandin E2 • Increased concentration of inflammatory metabolites from muscle contractions, including lactic acid, potassium chloride (Jovanovic et al 1990), arachidonic acid (Djupsjobacka et al 1994), bradykinin (Pedersen et al 1997) and 5-HT (Djupsjobacka et al 1995) results in increased gamma fibre activation and sensitivity of muscle spindles leading to increased stiffness. • Experimentally induced pain has been shown to be associated with changes in the fusimotor system (Thunberg et al 2002) • Neck and paraspinal muscles are rich in muscle spindles (Richmond & Abrahams 1975, Amonoo- Kuofi 1982, Boyd-Clark et al 2002). These spindles, many of which lack bag fibres, are controlled by the static fusimotor system and are mainly concerned with postural muscle activity (Price & Dutia 1989) and therefore disturbances in these fusimotor fibres are likely to cause disturbances in motor co-ordination and proprioception • Stimulation of fusimotor activity through the application of vibration to the neck muscles has been shown to cause disturbances in balance and motor activity (Lund 1980)Muscle hypoactivity and chronic pain • Clinical observation also suggest that there can be inhibition of muscle activity • An alternate model, ’the pain adaptation model’ proposes that muscle dysfunction is a normal protective adaptation and is not one of the causes of pain (Lund et al 1993) • Investigations suggest inhibition of the agonist and facilitation of the antagonist during walking thereby reducing movement amplitude and stride time during experimentally induced leg muscle pain (Graven-Nielsen et al 1997; Madeleine et al 1999) • Injection of hypertonic saline into one side of the erector spinae has been shown to reduce the velocity and range of voluntary trunk movements (Zedka et al 1999), where the concomitant reduction in EMG amplitude persisted even when subjects pushed through the discomfort • Patients with chronic low back pain fatigue faster (Kankaanpaa et al 1998) and have poorer balance performance and delayed postural response times (Radebold et al 2000, 2001) • In normal subjects, fatigue can result in altered anticipatory adjustments (Allison & Henry 2002)Wider effects • Injection of hypertonic saline into the trapezius muscle during low load repetitive work task not only resulted in reduced activity in the injected muscle but additionally altered rhythm, a tendency to increase the amplitude of arm movements and a prolongation of the role of the non-affected arm in the task (Madelaine et al 1999) • Injection of hypertonic saline into the soleus muscle altered gait and hence rhythm of other muscles in the synergy (Martin & Arendt-Nielsen 2000)

Models of Motor Control

• It is now realised that the distinctions made in the hierarchical model (upper motor neurones for purposeful action and lower motoneurons for reflexes) and the simple stretch reflex are insufficient to explain simple models of motor control as these distinctions become more and more blurred. For example every voluntary movement has a concomitant reflexogenic postural adjustment that occurs subconsciously • Central pattern generators (CPG) are derived from motor programs where a sequence of commands have been pre-programmed. • Examples of CPGs are rhythmical movements such as walking and respiration which are motor patterns that receive sensory feedback thereby making it a closed loop system • Open loop system require feedforward mechanisms which deliver information to other parts of the system to ‘prepare’ it for upcoming motor commands such as postural adjustments prior to limb movements • Bernstein (1967) perspective described movement constrained to synergies or coordinative structures (ie functional units of joints and muscle constrained to act as one) whereby control is not exerted over muscles or sensory receptors (reflex model) nor muscle activation patterns (hierarchical model) but rather over abstract relations between kinematic variables and the accomplishment of task goals • The Dynamic Action Theory (an elaboration on systems theories) proposes that movement emerges naturally out of complex interactions among many interconnected elements (physical, environmental and neural) without specific commands or motor programs in the CNS • At the core of dynamic action theory is that human behaviour is governed by a generic process of self-organisation; functionally linked rather than mechanically linked (Kelso & Tuller 1984), task dependent and constrained as units of action specified in dynamic terms rather than kinematic or muscular variables and determined by features of the action such as movement trajectory (Saltzman & Kelso 1987)

Nervous System Plasticity

• Cortical plasticity has been most dramatically demonstrated by Merzenich and colleagues (1983, 1984) whereby digital representation of the hand was remapped in the somatosensory cortex following deafferentation and digital amputation in monkeys. • In humans this re-organisation is not haphazard but context specific whereby the brain can be viewed as a dynamic entity (Kelso 1995) • Rapid repetitive highly stereotypical arm movements in monkeys were shown to degrade sensory representations of sensory information guiding fine motor hand movements leading to dystonia and subsequent lack of use of the hand (Byl et al 1996)

Dynamical View of Pain and Motor Control – Groups of cells rather than single cells are the main units of activity in the nervous system – Functional synergies of muscles rather than single muscles are then main units of motor control and coordination of action – There is distributed control of these systems Timing relationships between muscles appears to be the critical restraint rather than amplitude.

Chronic Pain and Motor Control

• Pain is essentially motoric, whereby the basic biological function of pain is to escape or prevent danger and promote survival (Melzack 1996, Wall & Melzack 1999) • Abnormal movement patterns can be compensatory to pain, causative of pain or neither • What defines chronic pain still has not been established – mechanisms/aetiology, duration, physiology • The complexities between chronic pain and movement concern the lack of understanding of the physiological complexities of chronic pain and the potent effects of cognitive and emotional factors • Allodynia has particular implications as non-noxious movements are now deemed painful suggesting that even small deficits in motor control may be sufficient to maintain a nociceptive input • Peripheral nerve injury can induce more robust peripheral hyperalgesia whereby small regenerating sprouts who don’t reach their target organ, turn back on themselves creating a small tangle of nerve fibres which can become ectopic impulse generators (Devor & Seltzer 1999, Wall & Gutnick 1974, Xie et al 1993) are sensitive to tension & compression, chemical substances as a result of anoxia and inflammation and noradrenaline (Janig et al 1996) • The dorsal root ganglia (DRG) may also become a source of ectopic generators whose afferent input can sensitise the dorsal horn of the spinal cord, and whose efferent input can create neurogenic inflammation which may result in secondary hyperalgesia • Unlike the rest of the peripheral nervous system, the dorsal root ganglion is particularly permeable to vascular circuits, thereby making circulating chemicals and humoral factors particularly accessible. This has important ramification to people in chronic pain who often suffer high levels of stress with the associated release of catecholamines • Finally, the DRG is situated close the intervertebral disc where damage to the disc can release inflammatory cytokines which may permeate into the DRG

Central Mechanisms of Chronic Pain

• Reduction of normal inhibitory inputs (‘disinhibition’) caused by removal of supraspinal projections to the WDR neuron can cause sensitization (Doubell et al 1999) suggesting that pain sensitisation can occur in the absence of peripheral mechanisms. Furthermore, increased descending facilitation of interneurons can also result in pain. • These changes are called central sensitization and manifest clinically as secondary hyperalgesia and allodynia which is produced from elevated resting membrane potential, reduced activation thresholds of the second order nociceptor, altered gene expression and sprouting at the receptive synapses (Dubner & Ruda 1992) • Cortical structures are known to undergo structural reorganisation in patients in whom no peripheral neuropathy is demonstrable. Herta Flor and colleagues (1997) investigated the extent of somatosensory activation in people with chronic low back pain by showing noxious stimulation to increase somatosensory activity as a function of the duration of their pain. However, other studies demonstrate variable results • The most consistent finding across studies is the activation of the anterior cingulate cortex (ACC) (Peyron et al 2000) which is thought to be important in anticipation of pain (Sawamoto et al 2000) and anxiety (Kimbrell et al 1999). The ACC appears to be constantly active in chronic pain (Hsieh et al 1995) • It seems that the ACC is part of the motor function whereby the brain makes sense of the nociceptive input according to what it should do about it (Wall 1999) • ACC is important in establishing an emotional valence to pain and co-ordinating the perception of bodily threat with other areas in selecting and planning the appropriate behavioural/motor response strategy (Price 2000). • The ACC projects directly to motor and supplementary motor areas (Price 2000), and receives direct inputs from reticular formation neurons having a relevance in escape behaviour and fear response (Willis 1985)

Anterior Cingulate Cortex (ACC)

• Factors that are thought to impart threat or emotional valence to pain are thought to have greater impact on motor control than factors that impart stimulus intensity or sensory qualities to pain. As cognitive and emotional factors contribute more to pain, so too the impact of pain on motor control increases (Price 2000) • The majority of pre-synaptic projections from the dorsal horn are from WDR neurons is significant in that sensitisation of the dorsal horn almost exclusively involves WDR neurones promoting escape type responses

Implication of neural changes

•The neural adaptation associated with many chronic pain situations can be demonstrated as normal adaptation in abnormal circumstances •Increased nociceptive sensitivity leaves a smaller kinetic margin for error •Tolerance to non-nociceptive input is reduced due to WDR sensitivity, therefore creating a fine line of just doing enough to promote strength, endurance and control without doing too much resulting in a so called ‘flare up’ typically associated with severe pain sometimes with paraesthesia and nausea •Cortically mediated modulation of nociception may be sufficient to increase and maintain pain where perceived threat and sense of vulnerability are central to this effect •Structural reorganisation of the CNS can result in inaccurate transmission of proprioceptive information, which may disrupt internal spatial representation of the body, thereby further compromising motor control

Motor control in reducing lost game time in Australian Rules Footballers

A motor programme delivered to elite Afl players was effective in retaining muscle size and function of the multifidus and transverse abdominis whilst reducing the number of games missed during the season (Hides et al 2012, Med Sc Sp Ex, 44, 6, 1141-1149)

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Neuroplasticity in Tendinopathy
by Martin Krause
A multitude of contributing factors to altered motor control must be addressed when treating tendon dysfunction. What we have failed to consider in the past when dealing with chronic or recurrent tendon issues are motor control problems encompassing corticospinal control of excitation and inhibition as well as belief systems about pain and contextual factors related to imaging.
Research by Ebonie Rio et al (2015) (BJSM Sept 25, 10.1136/bjsports-2015-095215) suggest that the pain state sets up an adaptive pathway whereby the ipsilateral kinetic chain is directly inhibited by reflexogenic pathways, as well as being inhibited by contralateral hemispheric activity. Simultaneously excitation is enhanced in the opposite limb as well as in antagonists...at least in the case of enhanced excitation of the hamstrings in quadricep tendinopathy. If this is true, then so much for training the contralateral limb for 'cross training' purposes! This may also explain why a lot of people seem to have "all their injuries on the same side" (of the body). Furthermore, they recommend enhancing corticospinal drive through the use of 30-60 second isometric holds at 70-80% MVC to load the muscle whilst using isokinetics to load the tendon. Moreover, they recommend the use of a metronome at 60bpm (stages 1 and 2) with a count of 3 up, 2 down for quads, and 2 up, 3 down for calf isokinetics to optimally engage corticospinal drive through the visual and auditory stimuli (also shown by Kohei et al 2012 for motor imagery and M1 stimulation) .....read more
Cortical mapping of infraspinatus muscle in chronic shoulder pain demonstrating higher motor thresholds (aMT= activation MT) and hence reduced excitability on the affected side (39 vs 35) (Ngomo et al 2015 Clinical Neurophysiol, 126, 2, 365-371)
Cortical mapping of pain and fear. Lots of overlap suggesting that taking away the fear from the pain with clear clinical explanations and a focused goal directed program using specific functional outcomes is important.
Individuals with patellofemoral pain (PFP) had reduced map volumes and an anterior shift in the M1 representations, greater overlap of the M1 representation and a reduction in cortical peaks across all three quadriceps (RF, VL, VMO) muscles compared with controls.(Te et al 2017 Pain Medicine, pnx036, https://doi.org/10.1093/pm/pnx036)
Uploaded : 18 October 2017 Read More

Mon09Oct2017

Imaging

Do I need a scan? "a picture tells a thousand words" - not really!
by Martin Krause
A scan, in it's self, will not improve anyone's condition. The purpose of a scan is to gain more information about the pathology. Sometimes this information may be irrelevant to the management of a patient's condition. For example, if you knocked your elbow on a door frame and suffered a bruise, which was already beginning to resolve, an ultrasound scan may show some minor soft tissue damage, but that was already obvious by the fact of the bruise, and the information gained from the scan has not helped nor changed the management of the bruise. Therefore, the main reason for getting a scan would be because there is concern that the presence of certain pathologies may lead to a change in the medical management. For example, sometimes a rolled ankle can be more than sprained ligaments, and may require surgey or immobilisation in a boot. If the therapists suspects this might be the case, then they will recommend or refer for a scan (probably an X-Ray) to check the integrity of the bones (especially the fibular and talar dome), because if there is no bony damage then the patient can be managed conservatively with taping, exercises, ultrasound, massage, joint mobilisations etc. However, if there is boney damage, for example, then it might be necessary for the ankle to be immobilised in a boot for three - six weeks, for example. This dramatically different medical management depends on the results of a scan, and it is therefore worth doing.
However, scans have no predictive value to the presence or severity of pain. Thirty-three articles reporting imaging ﬁndings, in the low back, for 3110 asymptomatic individuals were investigated for pathology. The prevalence of disk degeneration in asymptomatic individuals increased from 37% of 20-year-old individuals to 96% of 80-year-old individuals. Disk bulge prevalence increased from 30% of those 20 years of age to 84% of those 80 years of age. Disk protrusion prevalence increased from 29% of those 20 years of age to 43% of those 80 years of age. The prevalence of annular ﬁssure increased from 19% of those 20 years of age to 29% of those 80 years of age. (Brinjikji, W et al Spine Published November 27, 2014 as 10.3174/ajnr.A4173). Hence, the results of imaging need to be assessed within the context of the entire clinical picture. Frequently too much emphasis is placed on the imaging not only by the clinician but also by the patient. Some people react to pathology seen on scanning as an affirmation of their problem and can either use it to gain clarity and become better or conversely become worse. Moreover, some people find imaging with inconclusive results as a 'panic moment' - "no one knows what is wrong".
Similarly, ultrasound imaging of the tendond has good predictive diagnostic and aids in clinical reasoning when it comes to full tears. However, with partial tears it is a totally different 'ball game'. Ultrasound is highly user dependent, with specifically trained musculoskeletal radiologists able to produce high-quality images that may provide more clinically relevant information than those produced by clinicians with less experience in imaging. Sean Docking, a leading tendon researcher at Monash University, cited 7 authors who found pathological tendon chnages in 59% of asymptomatic individuals, whereas he found that 52% of asymptomatic elite AFL sportsmen had tendon pathology on imaging! Furthermore, symptomatic individuals who improved clinically to the point of resuming play, weren't shown to have improvements on imaging. Again, the clinical context and the clinical reasoning can in many instances prove to be the 'gold standard' not the imaging itself, when considering management options.
Shoulder supraspintatus tendon pathology, in the abscence of trauma, is known, in many instances, to be a disorder of immune-metabolic compromise of the tendon and bursa. Imaging may show some changes in signal intensity but, unless it's a complete tear, it can reveal neither the intensity nor the severity of pain when taken outside of the clinical context. A thorough physical and subjective examination integrating all the clinical dimensions of the problem will have far greater value than any one single imaging modality.
Yet, imaging still should be used in instances of progressive rapid deterioration and suspected serious pathology which may require surgery and/or immediate medical intervention.
In summary, sometimes it is worthwhile getting a scan, because the information gained from that scan will determined the type of medical management that is employed. However, at other times, the scan may be unneccessary, because the information may be irrelevant or lead to an incorrect change in medical management, due to over-reporting of 'false positives'. You will be able to make this decision on the advice of your health care professional. On occasions it can actually be detrimental to have a scan, because some patients can become overly obsessed with the medical terms used to describe their scan results, which then can become the major focus for the clinician and the patient, rather than the more prefereable focus on their symptoms and functional abilities. For example, many people have lumbar buldging discs yet have no symptoms, yet sometimes when these patients have an MRI or CT scan, they can develop symptoms because they think they should have pain if the scan says so! Conversely, for some people the results of imaging can have a positive and reassuring affect. Therefore, it is very important to assess a clients attitude to scans before prescibing them so that the patient's expectations are managed appropriately, and not burdened by the additional, sometimes confusing, information supplied by a scan.
Uploaded : 10 October 2017 Read More

Thu14Sep2017

Cervical Spine implications in concussion

Neck aetiology, autonomic and immune implications, exercise and diet in the musculoskeletal physiotherapy management of Post Concussion Syndrome (PCS)
by Martin Krause, MAPA, Titled member Musculoskeletal Physiotherapy Association of Australia
A 14 year old boy presented to A&E, in August 2016, after receiving an impact to the head during AFL (Australian Rules Football). Although his SCAT3 scores were relatively mild, he went on to suffer severe lethergy, resulting in a lengthy abscence from school, culminating in a return to school for exams in the first week of December 2016. Even by December, even a 30 minute walk was extremely fatiguing. To place this into perspective, he had been playing elite academy grade AFL for several seasons and was an extremely fit outdoor adventurer.
Confounding Variables :
end of season injury and hence no follow up from the academy
suffers from Hypermobile Joint Syndrome (HJS) and possibly Ehlers Danlos Syndrome (EDS), however Beighton score 4/9.
suffers from food intolerances, particularly to Glutin and diary, but also some other foods. Potential IBS and autoimmune issues.
had just gone through a growth spurt (190cm)
Imaging :
Brain MRI normal
Medical Examination :
Balance remained impaired to tandem walking and single leg stance. The vestibular occular motor scale showed significant accomodation deficit of 15cm and there was a mild exacerbation of symptoms. ImPACT testing revealed adequate scores and reaction time of 0.65 which is within acceptable range.
History :
School holidays December - January. Return to school and was placed in the lower classes. Prior to his concussion he was a top 10 student at an academically selective high school. Took up basketball and rowing as summer sports. Academic results tanked. Several Basketball injuries (Feb - April 17') as a result of what apppeared to be muscular imbalances from the relatively recent growth spurt, as well as taking on a new sport. Showed little interest in returning to AFL as no-one had followed him up during the previous year.
Current History :
September 2017 showed a continued decline in academic levels. School teachers noted an inability to concentrate. Academic results still well below pre-concussion levels. Fatigue continuing to be problematic.
Literature Review :
Post Concussion Syndrom (PCS) is defined as "cognitive deficits in attention or memory and at least three or more of the following symptoms: fatigue, sleep disturbances, headache, dizziness, irritability, affective disturbance, apathy, or personality change"
Further complications of PCS also appear to be an increased risk of musculoskeletal injury
Nordstrom et al (2014, BMJ Sports Med, 48, 19, http://bjsm.bmj.com/content/48/19/1447)
Predictors of PCS are uncertain. However, the following clinical variables are considered factors at increasing risk. These include prior history of concussion, sex (females more prominant), younger age, history of cognitive dysfunction, and affective disorders such as anxiety and depression (Leddy et al 2012, Sports Health, 4, 2, 147-154).
Unlike the 'good old days' which recommended a dark room and rest for several weeks post concussion, the consensus appears to be a graded return to exercise in order to restore metabolic homeostasis. Incredibly, highly trained young individuals can find even exercises in bed extremely demanding. Kozlowski et al (2013, J Ath Train, 48, 5, 627-635) used 34 people 226 days post injury to conclude significant physiological annomalies in response to exercise which may be the result of 'diffuse cerebral swelling'. Researchers have noted lower systolic and higher diastolic blood pressure in PCS (Leddy et al 2010, Clin J Sports Med, 20, 1, 21-27). Due to autonomic dysfunction manifested in altered cardiovascular and pulmonary responses (Mossberg et 2007, Arch Phys Med Rehab, 88, 3, 15-320) some clinicians have recommended the use of the exercise program for POTS (Postural Orthostatic Tachycardia Syndrome). This is a 5 month program which recommends mainly exercise in the horizontal and sitting positions for 1-4 months, including recumbent bike, rowing ergometer and swimming laps or kicking laps with a kick board. Month 4 upright bike and Month 5 upright training such as a elliptical trainer or treadmill.
http://www.dysautonomiainternational.org/pdf/CHOP_Modified_Dallas_POTS_Exercise_Program.pdf
Other progressive exercise therapies have also included 20 minutes per day, 6 days per week, for 12 weeks of either treadmill or home gym exercises at 80% of the heart rate at which their concussion symtoms are exacerbated. Their programs were individually modified as the heart rate provoking symptoms increased. When compared to the 'control group', this intervention was shown to improve cerebral perfusion on fMRI, increase exercise tolerance at a higher heart rate, less fatigue and were showing activation patterns in areas of the brain on performing math processing test which were now normalised (Leddy et al 2010, Clin J Sports Med, 20, 1, 21-27).
Graded exercises could also have included 'motor imagery' as espouse by the NOI group and the work of Lorrimer Moseley (University South Australia) when dealing with chronic pain.
Ongoing Symptoms :
The literature review by Leddy et al (2012) found that ongoing symptoms are either a prolonged version of concussion pathophysiology or a manifestation of other processes, such as cervical injury, migraine headaches, depression, chronic pain, vestibular dysfunction, visual disturbance, or some combination of conditions.
Physiotherapy Assessment :
One year PCS, fatigue continued to persist. Cognitive deficits with school work were reported to becoming more apparent. Assessment using various one leg standing tests employing oscillatory movement aroud the hips and knees for kinetic limb stability and lumbopelvic stability, which had been employed 6 months previously for his Basketball injuries were exhibiting deficits, despite these being 'somewhat good' previously.
Physical Examination : cervical and thoracic spine
Due to the Joint Hypermobility Syndrome (JHS) it was difficult to ascertain neck dysfunction based on range of movement testing. ROM were unremarkable except for lateral flexion which demonstrated altered intervertebral motion in both directions. Palpation using Australian and New Zealand manual therapy techniques such as passive accessory glides (upslopes and downslopes and traction) exhibited muscles spasms in the upper right cervical spine. In particular, the right C1/2 regions demonstrated most marked restrictions in movement. Eye - Neck proprioceptive assessment using blind folds and laser pointer also revealed marked variance from the normal. Repositioning error using the laser pointer with rotation demonstrated marked inability to reposition accurately from the left, tending to be short and at times completely missing the bullseye. Gaze stability with body rotation was NAD. Gaze stability whilst walking displayed some difficulty. Laser pointer tracing of the alphabet was wildly inaccurate. Thoracic ring relocation testing also revealed several annomalies, which may have also accounted for some autonomic dysfunction.
Occulomotor assessment and training
Upper Cervical Spine :
The upper cervical spine (atlas and axis) represents approximately 50% of the available rotation. An investigation into the environmental and physiological factors affecting football head impct biomechanics found that rotational acceleration was one of the few factors approaching significance and concluded that more research should be undertaken to evaluate this (Mihalik et al 2017 Med Sc Sp Ex, 49, 10, 2093-2101).
Headache :
Commonly referred to as cervicogenic headaches, one in five headaches in the general population are thought to be due to the cervical spine. The Upper Cervical Spine is particularly vulnerable to trauma because it is the most mobile part of the vertebral column, with a complex proprioceptive system connecting the vestibular apparatus and visual systems. It also coincides with the lower region of the brainstem and fourth ventricle. The brainstem houses many neurones associated with autonomic responses to pain and balance. Imaging of the fourth ventricle for swelling of the 'tonsils' and Arnold Chiari malformations are recommended when symptoms persist. In particular, children and adolescents are more vulnerable to neck contusions due to the proportionately larger head and less developed musculature. Cervical vertigo and dizziness after whiplash can mimic symptoms of PCS.. Mechanoreceptor dysfunction and vertebrobasilar artery insufficiency should be part of the differential diagnosis. Mechanical instability of the Upper Cervical Spine should also not be missed.
Cervicogenic Headaches
Further Interventions :
Neurocognitive rehabilitation of attention processes. Psychological intervention using cognitive behavioural therapy (CBT). Neuro-opthalmologist to assess and treat smooth pursuit eye tracking. Naturopath for food intolerances and dietician for the optimisation of diet.
Diet :
In cases with chronic fatiguing factors, nutrition can be become a vital aspect into the reparative process. This may include energy and mineral rich foods such as bananas, green leafy vegetables for iron and magnesium (200-300mg), oranges for vitamin C (anit-oxidant and helps with the absorption of iron), anti-oxidant rich foods such as EPA/DHA (1000mg) fish oil, curcumin (tumeric), Cats Claw, Devils Claw, Chia seeds, fruits of the forest (berries), and CoQ10 with Vitamin B. Folate and Ferritin levels should also be checked. Calorific energy intake should balance with energy exependiture. However, as we are often dealing with young individuals, as in this case, some form of comfort food may be appropriate such as, nuts, legumes, homus and sushi. Protein intake prior to carbohydrate intake may help ameliorate any blood suger fluctuations due to Glycemic Index factors, however simple carbohydrates (high GI) should be avoided wherever practical. Even oats need to be soaked overnight and cooked briefly, otherwise they become a high GI food and may even affect the absorption of iron. The type of rice used can also influence GI, hence the addition of protein such as fish. Protein supplementations are generally over-used. Daily protein intake should not exceed 1.2g per kg of body weight per day. Dosage for children is less than that for adults.
See Nutritional Section of this Site
Conclusion
Investigations, into people with persisting PCS, demonstrated that they applied more force over time to control balance. Helmich et al (2016, Med Sc Ex Sp, 48, 12, 2362-2368) proposed that in regard to cognitive processes, the increase of cerebral activation indicates an increase of attention demanding processes during postural control in altered environments. This is relevant in so far as individuals with post concussive symptomatology have a variety of symptoms including headache, dizziness, and cognitive difficulties that usually resolve over a few days to weeks. However, a subgroup of patients can have persistent symptoms which last months and even years. Complications in differential diagnosis, can arise clinically, when neck dysfunction and altered motor control occur concurrently due to both neck and cerebral pathology. For example, Whiplash and other traumatic head and neck injuries can result in pathology to both regions, whereas, more discreet altered cognitive processing from concussion can result in altered neck motor control. Musculoskelatal Physiotherapy can play a vital part in the treatment of neck dysfunction including the re-establishment of occulomotor proprioception and managing localized strength and cardiovascular exercise regimes. A total body, multi-disciplinary approach which is well co-ordinated amongst practitioners is vital to an optimal outcome.
Uploaded : 17 November 2017 Read More

Thu24Aug2017

Pain in the Brain - neural plasticity

Pain in the Brain and Neural Plasticity
by Martin Krause
There are several mechanisms that can create a sensation of pain, which has been described as 'an unpleasent sensory and emotional experience in response to perceived or potential tissue damage'. Pain can be the result of peripheral sensitisation from peripheral inflammation, vascular compromise, necrosis, swelling, etc. Importantly, higher centres of the central nervous system not only perceive such sensitization of the peripheral nerve receptors, they can also modulate and control the intensity and tolerability of the perceived sensation through descending modulation at the peripheral receptor and in the spinal cord and through transcortical mechanisms depending on the 'meaning' and 'context given to the pain. Moreoever, the higher centres can create a 'state' of perceived 'threat' to the body through emotions such as fear and anxiety. Rather than the brain acting as a filter of unwanted sensation, in the higher centre induced pain state, rumination and magnification of sensations occur to create a pathological state. Paradoxically, representation of body parts such as limbs and individual muscles can reduce in perceived size. In such instances the pain doesn't represent the sensation of pathology but rather pain has become the pathology. Hence, the brain generates pain in the brain, where the pain is perceived to be some sort of non-existant inflammatory or pathological sensation in the periphery. Evidence for this neural plasticity comes from imaging studies, where brain white matter structural properties have been shown to predict transition to chronic pain (Mansour et al 2013, Pain, 154, 10, 2160-2168). Specifically, differential structural connectivity to medial vs lateral prefrontal cortex and connectivity between medial prefrontal cortex and nucleus accumbens has been shown in people with persistent low back pain. In this case the back pain becomes the inciting event and given the persons' structural propensity, establishes specific functional coonectivity strength.
further reading
Peripheral input is a powerful driver to neuroplasticity. Information gathered by touch, movement and vision, in the context of pain can lead to mal-adaptive plasticity, including the reorganisation of the somatosensory, and motor cortices, altered cortical excitability and central sensitisation. Examples of somatosensory reorganisation come from the work of Abrahao Baptista when investigating chronic anterior knee pain, who not only demonstrated reduced volume of Vastus Medialis but also is cortical translocation to another part of the cortex.
ndividuals with patellofemoral pain (PFP) had reduced map volumes and an anterior shift in the M1 representations, greater overlap of the M1 representation and a reduction in cortical peaks across all three quadriceps (RF, VL, VMO) muscles compared with controls.(Te et al 2017 Pain Medicine, pnx036, https://doi.org/10.1093/pm/pnx036)
AKP = anterior knee pain
The same researcher (Abrahao Baptista) has shown that maximal tolerable electrical stimulation (eg TENS) of muscles can induce normalisation of the cortical changes through a process called 'smudging'. Transcortical stumilation has also been applied as a cortical 'primer' prior to the application of more traditional therapy such as motor re-training, exercise, and manipulation.
Body illusions are another novel way to promote the normalisation of cortical function through adaptive neuroplasticity. Examples come from people with hand athritis, whose perception of their hand size is underestimated (Gilpin et al 2015 Rheumatology, 54, 4, 678-682). Using a curved mirror, similar to that in theme parks, the visual input can be increased to perceive the body part as larger (Preston et al 2011 DOI: 10.1093/rheumatology/ker104 · Source:PubMed ) . Irrespective of size, watching a reflection of the hand while performing synchronised movements enhances the embodiment of the reflection of the hand (Whitkopf et al 2017, Exp Brain res, 23, 5, 1933-1944). These visual inputs are thought to affect the altered functional connectivity between areas of the brain thereby affecting the 'pain matrix'.
Another, novel way of looking at movement and pain perception is the concept of the motor engram. This has been defined as motor skill acquisition through the modification and organisation of muscle synergies into effective movement sequences. The learning process is thought to be acquired as a child through experientially based play activity. The specific neural mechanisms involved are unknown, however they are thought to include
motor map topography reflecting the capacity for skilled movement
reorganisation of motor maps in a manner that reflects the kinematics of aquired skilled movement
map plasticity is supported by a reorganisation of cortical microcircuitry involving changes in synaptic efficacy
motor map integrity and topography are influenced by various neurochemical signals that coordinate changes in cortical circuitry to encode motor experience (Monfils 2005 Neuroscientist, 11, 5, 471-483).
Interestingly, it is an intriguing notion that accessing motor engrams from patterns aquired prior to the pain experience might lead a normalisation of brain activity. My personal experience of severe sciatica with leg pain, sleepness nights and a SLR of less than 30 degrees, happened to coincide with training my 9 year old sons soccer training. I was noticing that the nights after i trained the children, I slept much better and my range of movement improved. I commenced a daily program of soccer ball tricks which i had been showing the kids, including 'juggling', 'rainbows' and 'around the worlds'. Eventually, I even took up playing soccer again after a 30 year abscence from the sport. Other than new activity related pain issues (DOMS), four years on, the sciatica hasn't returned. I can only conclude that this activity activated dormant childhood motor engram, worked on global balance, mobilised my nerve, encouraged cross cortical activity and turned my focus into finctional improvement.
Further explainations for my expereience comes from evidence suggesting that a peripheral adaptive pain state is initiated, whereby transcortical inhibiton occurs by the contralaleral hemisphere to the one which controls the affected limb. Additionally, excitation cortical (M1) drive of the muscles of the contralateral limb to the one which is in pain also occurs. In such cases re-establishement of motor drive to the affected side is important. In terms of tendon rehabilitation, external audtory and visual cues using a metronome have been employed and are showing promising results (Ebonie Rio et al 2017 Personal communication). In terms of my experience with the soccer ball tricks, the external visual cues and the cross talk from using left and right feet, head, shoulders, and chest during ball juggling manouvers, whilst calling the rhythm to the kids may have been the crucial factor to overcome the dysfunctional brain induced pain - muscle inco-ordination cycle, which I was in. Additionally, I was cycling which allowed me to focus on motor drive into the affected.limb.
However, work by Lorrimer Moseley on CRPS has established that 'brain laterality' must be established before commencing trans-cortical rehabilitation techniques. Lorrimer's clinical interventions use 'mirror imaging' techniques which are only effective once the patient is able to discriminate the left and right sides of the affected body parts, presented visually, in various twists and angles.
Alternatively, the altered pain state can result in a hostage like situation, whereby the pain takes control. Similar to the 'Stockholm Syndrome' where the hostage begins to sympathise with their captors, so do some peoples brain states, where it begin to sympathise with the pain, creating an intractable bondage and dysfunctional state.
One screening question which may reflect commitment to the process of rehabilitatation is to question whether they were able to resist the cookie jar when they were a child? Or were they committed to any sporting endeavours as a child? This may give some indication for the presence of motor engrams which can be used to overcome dysfunctional pain induced muscle synergies (neurotags), but also indicate an ability to be self disciplined, as well as being able to reconcile and identify goal oriented objectives, in spite of the cognitive pain processes? Remember that neurons that fire together, wire together.
Uploaded : 18 October 2017 Read More

Thu03Aug2017

Sickle Cell Trait and Acute Low Back Pain

Researchers believe that lumbar paraspinal myonecrosis (LPSMN) may contribute to the uncommon paraspinal compartment syndrome and that sickle cell trait (SCT) may play a role. Sustained, intense exertion of these lumbar paraspinal muscles can acutely increase muscle size and compartment pressure and so decrease arterial perfusion pressure. This same exertion can evoke diverse metabolic forces that in concert can lead to sickling in SCT that can compromise perfusion in the microvasculature of working muscles. In this manner, they believe that SCT may represent an additional risk factor for LPSMN. Accordingly, they presented six cases of LPSMN in elite African American football players with SCT. See link below
http://journals.lww.com/acsm-msse/Fulltext/2017/04000/Acute_Lumbar_Paraspinal_Myonecrosis_in_Football.1.aspx Read More

Mitochondrial Health and Sarcopenia

The aging process (AKA 30 years of age onwards), in the presence of high ROS (reactive oxygen species) and/or damaged mitochondrial DNA, can induce widespred mitochondrial dysfunction. In the healthy cell, mitophagy results in the removal of dysfunctional mitochondria and related material. In the abscence of functional removal of unwanted mitochondrial material, a retrograde and anterograde signalling process is potentially instigated, which results in both motor neuronal and muscle fibre apoptosis (death) (Alway, Mohamed, Myers 2017, Ex Sp Sc Rev, 45, 2, 58-69). This process is irreversible. Investigations in healthy populations, have shown that regular exercise improves the ability to cope with regular oxidative stress by the buffering and 'mopping up' of ROS agents which are induced as a result of exercise. It is plausible and highly probable that regular exercise throughout life can mitigate against muscle fibre death (Sarcopenia). Importantly, this process of muscle fibre death can commence in the 4th decade of life. and be as much as 1% per year. Reduction of muscle mass can result in immune and metabolic compromise, including subclinical inflammation, type II diabetes as well as the obvious reduction in functional capacity for activities of daily living.
Published 11 July 2017 Read More

Thu22Dec2016

Ehlers Danlos Syndrome

Is your child suffering Ehlers Danlos Syndrome? Hypermobile joints, frequent bruising, recurrent sprains and pains? Although a difficult manifestation to treat, physiotherapy can help.
Joint Hypermobility Syndrome (JHS)
by Martin Krause
When joint hypermobility coexists with arthralgias in >4 joints or other signs of connective tissue disorder (CTD), it is termed Joint Hypermobility Syndrome (JHS). This includes conditions such as Marfan's Syndrome and Ehlers-Danlos Syndrome and Osteogenesis imperfecta. These people are thought to have a higher proportion of type III to type I collagen, where type I collagen exhibits highly organised fibres resulting in high tensile strength, whereas type III collagen fibres are much more extensible, disorganised and occurring primarily in organs such as the gut, skin and blood vessels. The predominant presenting complaint is widespread pain lasting from a day to decades. Additional symptoms associated with joints, such as stiffness, 'feeling like a 90 year old', clicking, clunking, popping, subluxations, dislocations, instability, feeling that the joints are vulnerable, as well as symptoms affecting other tissue such as paraesthesia, tiredness, faintness, feeling unwell and suffering flu-like symptoms. Autonomic nervous system dysfunction in the form of 'dysautonomia' frequently occur. Broad paper like scars appear in the skin where wounds have healed. Other extra-articular manifestations include ocular ptosis, varicose veins, Raynauds phenomenon, neuropathies, tarsal and carpal tunnel syndrome, alterations in neuromuscular reflex action, development motor co-ordination delay (DCD), fibromyalgia, low bone density, anxiety and panic states and depression. Age, sex and gender play a role in presentaton as it appears more common in African and Asian females with a prevalence rate of between 5% and 25% . Despite this relatively high prevalence, JHS continues to be under-recognised, poorly understood and inadequately managed (Simmonds & Kerr, Manual Therapy, 2007, 12, 298-309). In my clinical experience, these people tend to move fast, rely on inertia for stability, have long muscles creating large degrees of freedom and potential kinetic energy, resembling ballistic 'floppies', and are either highly co-ordinated or clumsy. Stabilisation strategies consist of fast movements using large muscle groups. They tend to activities such as swimming, yoga, gymnastics, sprinting, strikers at soccer. Treatment has consisted of soft tissue techniques similar to those used in fibromyalgia, including but not limited to, dry needling, myofascial release and trigger point massage, kinesiotape, strapping for stability in sporting endeavours, pressure garment use such as SKINS, BSc, 2XU, venous stockings. Effectiveness of massage has been shown to be usefull in people suffering from chronic fatigue syndrome (Njjs et al 2006, Man Ther, 11, 187-91), a condition displaying several clinical similarities to people suffering from EDS-HT. Specific exercise regimes more attuned to co-ordination and stability (proprioception) than to excessive non-stabilising stretching. A multi-modal approach including muscle energy techniques, dry needling, mobilisations with movement (Mulligans), thoracic ring relocations (especially good with autonomic symptoms), hydrotherapy, herbal supplementaion such as Devils Claw, Cats Claw, Curcumin and Green Tee can all be useful in the management of this condition. Additionally, Arnica cream can also be used for bruising. Encouragment of non-weight bearing endurance activities such as swimming, and cycling to stimulate the endurance red muscle fibres over the ballistic white muscles fibres, since the latter are preferably used in this movement population. End of range movements are either avoided or done with care where stability is emphasized over mobility. People frequently complain of subluxation and dislocating knee caps and shoulders whilst undertaking a spectrum of activities from sleeping to sporting endeavours. A good friend of mine, Brazilian Physiotherapist and Researcher, Dr Abrahao Baptista, has used muscle electrical stimulation on knees and shoulders to retrain the brain to enhance muscular cortical representation which reduce the incidence of subluxations and dislocations.
Abrahao wrote : "my daughter has a mild EDS III and used to dislocate her shoulder many times during sleeping. I tried many alternatives with her, including strenghtening exercises and education to prevent bad postures before sleeping (e.g. positioning her arm over her head). What we found to really help her was electrostimulation of the supraspinatus and posterior deltoid. I followed the ideas of some works from Michael Ridding and others (Clinical Neurophysiology, 112, 1461-1469, 2001; Exp Brain Research, 143, 342-349 ,2002), which show that 30Hz electrostim, provoking mild muscle contractions for 45' leads to increased excitability of the muscle representation in the brain (at the primary motor cortex). Stimulation of the supraspinatus and deltoid is an old technique to hemiplegic painful shoulder, but used with a little different parameters. Previous studies showed that this type of stimulation increases brain excitability for 3 days, and so we used two times a week, for two weeks. After that, her discolcations improved a lot. It is important to note that, during stimulation, you have to clearly see the humerus head going up to the glenoid fossa"
Surgery :
The effect of surgical intervention has been shown to be favourable in only a limited percentage of patients (33.9% Rombaut et al 2011, Arch Phys Med Rehab, 92, 1106-1112). Three basic problems arise. First, tissues are less robust; Second, blood vessel fragility can cause technical problems in wound closure; Third, healing is often delayed and may remain incomplete.
Voluntary Posterior Shoulder Subluxation : Clinical Presentation
A 27 year old male presented with a history of posterior shoulder weakness, characterised by severe fatigue and heaviness when 'working out' at the gym. His usual routine was one which involved sets of 15 repetitions, hence endurance oriented rather than power oriented. He described major problems when trying to execute bench presses and Japanese style push ups.
https://youtu.be/4rj-4TWogFU
In a comprehensive review of 300 articles on shoulder instability, Heller et al. (Heller, K. D., J. Forst, R. Forst, and B. Cohen. Posterior dislocation of the shoulder: recommendations for a classification. Arch. Orthop. Trauma Surg. 113:228-231, 1994) concluded that posterior dislocation constitutes only 2.1% of all shoulder dislocations. The differential diagnosis in patients with posterior instability of the shoulder includes traumatic posterior instability, atraumatic posterior instability, voluntary posterior instability, and posterior instability associated with multidirectional instability. Laxity testing was performed with a posterior draw sign. The laxity was graded with a modified Hawkins scale : grade I, humeral head displacement that locks out beyond the glenoid rim; grade II, humeral displacement that is over the glenoid rim but is easily reducable; and grade III, humeral head displacement that locks out beyond the glenoid rim. This client had grade III laxity in both shoulders. A sulcus sign test was performed on both shoulders and graded to commonly accepted grading scales: grade I, a depression <1cm: grade 2, between 1.5 and 2cm; and grade 3, a depression > 2cm. The client had a grade 3 sulcus sign bilaterally regardless if the arm was in neutral or external rotation. The client met the criteria of Carter and Wilkinson for generalized liagmentous laxity by exhibiting hyperextension of both elbows > 10o, genu recurvatum of both knees > 19o, and the ability to touch his thumbto his forearm
Headaches
Jacome (1999, Cephalagia, 19, 791-796) reported that migraine headaches occured in 11/18 patients with EDS. Hakim et al (2004, Rheumatology, 43, 1194-1195) found 40% of 170 patients with EDS-HT/JHS had previously been diagnosed with migraine compared with 20% of the control population. in addition, the frequency of migraine attacks was 1.7 times increased and the headache related disability was 3.0 times greater in migraineurs with EDS-HT/JHS as compared to controls with migraine (Bendick et al 2011, Cephalgia, 31, 603-613).
People suffering from soft tissue hypermobility, connective tissue disorder, Marfans Syndrome, and Ehler Danlos syndrome may be predisposed to upper cervical spine instability. Dural laxity, vascular irregularities and ligamentous laxity with or without Arnold Chiari Malformations may be accompanied by symptoms of intracranial hypotension, POTS (postural orthostatic tachycardia syndrome), dysautonomia, suboccipital "Coat Hanger" headaches (Martin & Neilson 2014 Headaches, September, 1403-1411). Scoliosis and spondylolisthesis occurs in 63% and 6-15% of patients with Marfans syndrome repsectively (Sponseller et al 1995, JBJS Am, 77, 867-876). These manifestations need to be borne in mind as not all upper cervical spine instabilities are the result of trauma. Clinically, serious neurological complications can arise in the presence of upper cervical spine instability, including a stroke or even death. Additionally, vertebral artery and even carotid artery dissections have been reported during and after chiropractic manipulation. Added caution may be needed after Whiplash type injuries. The clinician needs to be aware of this possibility in the presence of these symptoms, assess upper cervical joint hypermobility with manual therapy techniques and treat appropriately, including exercises to improve the control of musculature around the cervical and thoracic spine. Atlantoaxial instability can be diagnosed by flexion/extension X-rays or MRI's, but is best evaluated by using rotational 3D CT scanning. Surgical intervention is sometimes necessary.
An interesting case of EDS and it's affect on post concussion syndrome can be read elsewhere on this site.
Temperomandibular Joint (TMJ) Disorders
The prevelence of TMJ disorders have been reported to be as high as 80% in people with JHD (Kavucu et al 2006, Rheum Int., 26, 257-260). Joint clicking of the TMJ was 1.7 times more likely in JHD than in controls (Hirsch et al 2008, Eur J Oral Sci, 116, 525-539). Headaches associated with TMJ disorders tend to be in the temporal/masseter (side of head) region. TMJ issues increase in prevelence in the presence of both migraine and chronic daily headache (Goncalves et al 2011, Clin J Pain, 27, 611-615). I've treated a colleague who spontaneously dislocated her jaw whilst yawning at work one morning. stressful for me and her! Generally, people with JHD have increased jaw opening (>40mm from upper to lower incisors).
Updated 17 October 2017 Read More

Fri09Dec2016

Physiotherapy with Sharna Hinchliff

Physiotherapy with Sharna Hinchliff
Martin is pleased to welcome the very experienced physiotherapist Sharna Hinchliff to Back in Business Physiotherapy for one on one physiotherapy sessions with clients in 2017. Sharna is a passionate triathelete and mother and has had several years experience working locally and internationally (New York and London) in the field of physiotherapy. Originally from Western Australia, Sharna graduated from the world renowned Masters of Manipulative Physiotherapy at Curtin University.
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Updated : 10 May 2014

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